It has been suggested that the natriuresis and diuresis accompanying the administration of vasodilators may be mediated through the kallikrein-kinin system. Preliminary studies involving the effect of infusions of PGE2, bradykinin, and dopamine on the excretion of urinary kallikrein were performed. Infusion of any one of the above vasodilators failed to produce any significant and consistent change in urinary kallikrein excretion.